A Reproducible Venous Thrombosis Model in Horses Induced by the Combination of an Endothelial Lesion and Blood Flow Stasis

Because of the high incidence of thromboembolic diseases in humans, experimental models of thrombosis have been widely developed in different animal species. The pathogenesis of thrombosis is associated with three components, first outlined by Virchow in 1856: vessel injury, stasis, and hypercoagulability. Based on this concept, the purpose of the present investigation was to create an innovative model of jugular thrombophlebitis in horses that included components of Virchow's triad and excluded surgical procedures. Eighteen horses were subjected to blood vessel injury through the coadministration of sclerosing agents (glucose and ethanolamine oleate) and transitory occlusion of the jugular flow by manual compression. Thrombus formation was followed by ultrasonography imaging, and all horses developed jugular thrombophlebitis, showing that the proposed model was effective. Once occlusive thrombophlebitis was induced, jugular venous pressure cranial to the lesion was evaluated and yielded increased values, suggesting cephalic hypertension. Biochemical tests were performed to verify hepatotoxicity and nephrotoxicity after the ethanolamine injection, but no abnormalities were observed. Five horses were then euthanized to evaluate the vascular, hepatic, and renal tissues. The jugular vein wall had increased thickness, inflammatory cell influx, endothelial destruction, and thrombus firmly adhered to the vessel intima. Histological evaluation of the hepatic and renal tissues was normal. The present thrombophlebitis model in the jugular vein of the horse is simple and reproducible, providing a useful tool for investigating acute and chronic venous thrombosis because the model allows evaluation of different aspects of the prevention, pathogenesis, and treatment of this disease.